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  • 1.
    Blackwood, Sarah J
    et al.
    Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet.
    Katz, Abram
    Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet.
    Isoproterenol enhances force production in mouse glycolytic and oxidative muscle via separate mechanisms.2019Ingår i: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 471, nr 10, s. 1305-1316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Fight or flight is a biologic phenomenon that involves activation of β-adrenoceptors in skeletal muscle. However, how force generation is enhanced through adrenergic activation in different muscle types is not fully understood. We studied the effects of isoproterenol (ISO, β-receptor agonist) on force generation and energy metabolism in isolated mouse soleus (SOL, oxidative) and extensor digitorum longus (EDL, glycolytic) muscles. Muscles were stimulated with isometric tetanic contractions and analyzed for metabolites and phosphorylase activity. Under conditions of maximal force production, ISO enhanced force generation markedly more in SOL (22%) than in EDL (8%). Similarly, during a prolonged tetanic contraction (30 s for SOL and 10 s for EDL), ISO-enhanced the force × time integral more in SOL (25%) than in EDL (3%). ISO induced marked activation of phosphorylase in both muscles in the basal state, which was associated with glycogenolysis (less in SOL than in EDL), and in EDL only, a significant decrease (16%) in inorganic phosphate (Pi). ATP turnover during sustained contractions (1 s EDL, 5 s SOL) was not affected by ISO in EDL, but essentially doubled in SOL. Under conditions of maximal stimulation, ISO has a minor effect on force generation in EDL that is associated with a decrease in Pi, whereas ISO has a marked effect on force generation in SOL that is associated with an increase in ATP turnover. Thus, phosphorylase functions as a phosphate trap in ISO-mediated force enhancement in EDL and as a catalyzer of ATP supply in SOL.

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  • 2.
    Fainstein, Nina
    et al.
    Hadassah - Hebrew University Medical Center, Jerusalem, Israel.
    Tyk, Reuven
    Ariel University, Ariel, Israel.
    Touloumi, Olga
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Lagoudaki, Roza
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Goldberg, Yehuda
    Ariel University, Ariel, Israel.
    Agranyoni, Oryan
    Ariel University, Ariel, Israel.
    Navon-Venezia, Shiri
    Ariel University, Ariel, Israel.
    Katz, Abram
    Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet.
    Grigoriadis, Nikolaos
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Ben-Hur, Tamir
    Hadassah - Hebrew University Medical Center, Jerusalem, Israel.
    Einstein, Ofira
    Ariel University, Ariel, Israel..
    Exercise intensity-dependent immunomodulatory effects on encephalomyelitis.2019Ingår i: Annals of Clinical & Translational Neurology, ISSN 2328-9503, Vol. 6, nr 9, s. 1647-1658Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Exercise training (ET) has beneficial effects on multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the intensity-dependent effects of ET on the systemic immune system in EAE remain undefined.

    OBJECTIVE: (1) To compare the systemic immune modulatory effects of moderate versus high-intensity ET protocols in protecting against development of EAE; (2) To investigate whether ET affects autoimmunity selectively, or causes general immunosuppression.

    METHODS: Healthy mice performed moderate or high-intensity treadmill running programs. Proteolipid protein (PLP)-induced transfer EAE was utilized to examine ET effects specifically on the systemic immune system. Lymph node (LN)-T cells from trained versus sedentary donor mice were transferred to naïve recipients and EAE severity was assessed, by clinical assessment and histopathological analysis. LN-T cells derived from donor trained versus sedentary PLP-immunized mice were analyzed in vitro for proliferation assays by flow cytometry analysis and cytokine and chemokine receptor gene expression using real-time PCR. T cell-dependent immune responses of trained versus sedentary mice to the nonautoantigen ovalbumin and susceptibility to Escherichia coli-induced acute peritonitis were examined.

    RESULTS: High-intensity training in healthy donor mice induced significantly greater inhibition than moderate-intensity training on proliferation and generation of encephalitogenic T cells in response to PLP-immunization, and on EAE severity upon their transfer into recipient mice. High-intensity training also inhibited LN-T cell proliferation in response to ovalbumin immunization. E. coli bacterial counts and dissemination were not affected by training.

    INTERPRETATION: High-intensity training induces superior effects in preventing autoimmunity in EAE, but does not alter immune responses to E. coli infection.

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